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By Douglas W. P. Hay (auth.), Dr. David Raeburn, Dr. Mark A. Giembycz (eds.)

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Brink C, Gillard V, Roubert P, Mencia-Huerta JM, Chabrier PE, Braquet P et al. Effects and specific binding sites of endothelin in human lung preparations. Pulmon. Pharmacol. 1991; 4: 54-9. 134. McKay KO, Black JL, Diment LM, Armour CL. Functional and autoradiographic studies of endothelin-I and endothelin-2 in human bronchi, pulmonary arteries, and airway parasympathetic ganglia. J. Cardiovasc. Pharm. 1991; 17 (Suppl. 7): S206-9. 135. Wu T, Rieves RD, Larivee P, Logun C, Lawrence MG, Shelhamer JH.

BioI. Chern. 1992; 267: 20551-4. 119. Lippton HL, Hauth TA, Cohen GA, Hyman AL. Functional evidence for different endothelin receptors in the lung. 1. Appl. Physiol. 1993; 75: 38-48. 120. Saeki T, Ihara M, Fukuroda T, Yamagiwa M, Yano M. 15 jEndothelin-l analogs with ET B agonistic activity. Biochem. Biophys. Res. Comm. 1991; 179: 286-92. 121. Takai M, Umemura I, Yamasaki K, Watakabe T, Fujitani Y, Oda K et al. 15 j-Endothelin-1 (8-21), IRL 1620, for the ETB receptor. Biochem. Biophys. Res. Comm.

Intravenous ET-l was reported to be a potent constrictor of canine airway circulation [234]. BQ-123 (1 IlM) markedly inhibited ET-I-induced vasoconstriction in rabbit perfused lungs but did not affect ET-l induced vasodilatation or hydrostatic oedema, or ET-3-induced vasoconstriction or hydrostatic oedema suggesting that these latter phenomena are mediated via non-ETA receptor-linked mechanisms [235]. Exposure of rats to a hypoxia atmosphere (10% O 2 ) for 3 weeks abolished, in a reversible manner, the pulmonary vasodilatation in perfused lungs that was normally elicited by ET-l or ET-3 in tissues from control animals (exposed to room air) [168].

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